{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T01:36:38Z","timestamp":1766367398713,"version":"3.48.0"},"reference-count":52,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,9,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Endotoxin tolerance (ET) has been demonstrated to attenuate the inflammatory response in murine models of sepsis. This study seeks to elucidate the underlying mechanisms by which ET modulates inflammation in sepsis, with a particular focus on macrophage autophagy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      An\n                      <jats:italic>in vivo<\/jats:italic>\n                      sepsis model was generated using cecal ligation and perforation, while an\n                      <jats:italic>in vitro<\/jats:italic>\n                      model of inflammatory injury was induced via lipopolysaccharide (LPS) administration. ET was established through pretreatment with low-dose LPS. Subsequent analyses were conducted to assess the presence of the NLRP3 inflammasome, autophagic flux, and the expression levels of TRIM26.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Heightened inflammation was observed in the TNF-\u03b1 levels and various organs of the sepsis group; conversely, inflammation was reduced in the group receiving ET treatment. Upon stimulation with LPS, primary mouse peritoneal macrophages exhibited activation of the NLRP3 inflammasome and autophagy, accumulation of mitochondrial reactive oxygen species, compromised membrane potential, resulting in cell apoptosis, and decreased expression of TRIM26. ET was found to enhance autophagy, suppress the activation of NLRP3 inflammasomes, and upregulate the expression of TRIM26. Interestingly, modulation of autophagy levels either reversed or intensified the protective effects of ET on macrophages\n                      <jats:italic>in vitro<\/jats:italic>\n                      . Knockdown of TRIM26 using small interfering RNA (siRNA) resulted in increased NLRP3 inflammasome activation and accumulation of P62.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We reveal that ET restores the autophagic flux in macrophages, inhibit NLRP3 inflammasome activation, and mitigate inflammatory damage in septic mice, potentially through the regulation of TRIM26.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1515\/med-2025-1231","type":"journal-article","created":{"date-parts":[[2025,9,3]],"date-time":"2025-09-03T12:58:16Z","timestamp":1756904296000},"source":"Crossref","is-referenced-by-count":0,"title":["Endotoxin tolerance inhibits NLRP3 inflammasome activation in macrophages of septic mice by restoring autophagic flux through TRIM26"],"prefix":"10.1515","volume":"20","author":[{"given":"Yanyan","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Ultrasonography, Nanjing Hospital of Traditional Chinese Medicine , Nanjing , Jiangsu , China"},{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shiwen","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Minghao","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xueting","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huifang","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Youran","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shanshan","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuchun","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sijie","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chibin","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, The First Affiliated Hospital of Ningbo University , Ningbo , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naibin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Ningbo University , No. 59 Liuting Road , Ningbo , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mingqin","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"},{"name":"Consortium for Infection and Innovation (CII), The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2025,9,3]]},"reference":[{"key":"2025122201304622923_j_med-2025-1231_ref_001","doi-asserted-by":"crossref","unstructured":"Ford JS, Morrison JC, Kyaw M, Hewlett M, Tahir P, Jain S, et al. 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